Mouse anti-Human BCL2 polyclonal antibody

Background Global ischemia is the resulting effect of a cardiopulmonary arrest (CPA). Presently there is no effective treatment to address neurological deficits in patients who survived a CPA. Granulocyte-colony stimulating factor is a growth factor (G-CSF) with a plethora of beneficial effects, including neuroprotection. Clinical application of human G-CSF (hG-CSF) is limited due to its plasma half-life of 4 h. Therefore, novel approaches need to be investigated that would (1) enable prolonged manifestation of hG-CSF and (2) demonstrate G-CSF efficacy from studying the underlying protective mechanisms of hG-CSF. In our previous work, we used the self-complementary adeno-associated virus (stereotype2: scAAV2) as a vector to transfect the hG-CSF gene into the global ischemic brain of a mouse. As an extension of that work, we now seek to elucidate the protective mechanisms of hG-CSF gene therapy against endoplasmic reticulum induced stress, mitochondrial dynamics and autophagy in global ischemia. Method A single drop of either AAV-CMV-hG-CSF or AAV-CMV-GFP was dropped into the conjunctival sac of the Swiss Webster mouse's left eye, 30-60 min after bilateral common artery occlusion (BCAO). The efficacy of the expressed hG-CSF gene product was analyzed by monitoring the expression levels of endoplasmic reticulum stress (ER), mitochondrial dynamics and autophagic proteins over 4- and 7-days post-BCAO in vulnerable brain regions including the striatum, overlying cortex (frontal brain regions) and the hippocampus (middle brain regions). Statistical analysis was performed using mostly One-Way Analysis of variance (ANOVA), except for behavioral analysis, which used Repeated Measures Two-Way ANOVA, post hoc analysis was performed using the Tukey test. Results Several biomarkers that facilitated cellular death, including CHOP and GRP78 (ER stress) DRP1 (mitochondrial dynamics) and Beclin 1, p62 and LC3-ll (autophagy) were significantly downregulated by hG-CSF gene transfer. hG-CSF gene therapy also significantly upregulated antiapoptotic Bcl2 while downregulating pro-apoptotic Bax. The beneficial effects of hG-CSF gene therapy resulted in an overall improvement in functional behavior. Conclusion Taken together, this study has substantiated the approach of sustaining the protein expression of hG-CSF by eye drop administration of the hG-CSF gene. In addition, the study has validated the efficacy of using hG-CSF gene therapy against endoplasmic reticulum induced stress, mitochondrial dynamics and autophagy in global ischemia.

Furan is an endocrine-disruptive chemical formed as a result of foods heat treatment as coffee, jarred and canned foods. It induces harmful effects on organisms. This study was intended to evaluate the effect of furan exposure on ovary, as a new rat polycystic ovary model (PCO), and the possible anti-inflammatory, anti-apoptotic and estrogenic effects of red clover (RC) dry extracts on it. Sixty adult female rats were divided into five groups (Control, RC, Furan, Protected and Treated groups). At the end of the experiment, Ovarian tissues were taken for histological (Hx & E and Picro - Sirius red stains), immunohistochemical (Bcl2, Er-beta & COX-2 immunoexpression), statistical & morphometrical studies. The ovarian sections of Furan group showed significant decrease in the number of the follicles and corpora lutea, follicular degeneration as well as many cysts and significant increased deposition of collagen fibers between the theca cells extending to the medulla. Bcl-2 and Er-beta immunoexpression were significantly decreased. However, the surface area percentage of COX-2 immunostain was significantly increased as compared to the control. The ovarian sections of the protected and treated groups with RC showed improvement in the histological and immunohistochemical alterations of furan induced ovarian injury. However, the treated group is significantly different from the protected group. It could be concluded that RC is more effective as a protected than treated agent against ovarian injury induced by furan.